Several studies suggest that gastritis, gastric ulcer and stress ulcer result from disruption of the ability of the mucosa to handle back diffusion H ion. Although a variety of agents have been shown to increase mucosal permeability and alter the buffering capacity of the mucosa, little is known about the machanism(s) which allow the stomach to maintain a high transmural to H ion. Recent studies suggest that the carboxyl group of salicylate is key to its damaging effects on the gastric mucosa. The relationships between the metabolic and permeability effects induced by salicylate, however, are not clear in terms of resulting ulceration. A great deal of attention has been recently paid to HCO3 secretion by gastric mucosa, which is also affected by salicylates. Recent data suggest that Hl receptor antagonists may be useful in further elaborating the importance of HCO3 secretion by gastric mucosa in order to protect itself against injury. There are additional compounds which seem to cause mucosal retention of the "alkaline tide". This study will continue to examine the effects of salicylate on the gastric mucosa in order to further define its mechanisms of injury. The importance of the surface cells secreting HCO3 will also be determined. The results will allow determination of mechanisms for maintanence and alterations of mucosal permeability. In addition to gaining insight as to the nature of the ability of the stomach to protect itself against acid, this investigation will also result in a better understanding of the complex interrelationship among ion transport processes in the stomach as well as metabolic regulation of ion transport in both fundus and antrum.